Binding of factor VIII-von Willebrand factor to human arterial subendothelium precedes increased platelet adhesion and enhances platelet spreading.
Time-dependent studies of platelet adhesion and binding of F VIII-VWF to human arterial subendothelium were carried out in vitro, using 51Cr-labeled platelets and 125I-labeled F VIII-VWF. Rapid binding of F VIII-VWF was found, resulting in a constant surface concentration after 1 to 2 min of perfusion. The number of platelets adhering in the first minute is similar in the absence of F VIII-VWF, but the platelet coverage is about twofold higher perfusions of 2 to 5 min in the presence of F VIII-VWF. Thus binding of F VIII-VWF precedes the increase in platelet adhesion, in line with our previous studies on the role of subendothelium-bound F VIII-VWF. By morphological evaluation it was found that the number of contact platelets (nonspread platelets) is lower in the presence of F VIII-VWF. The ratio of contact platelets to spread decreases in time, however, at a higher rate when F VIII-VWF is present. This indicates that F VIII-VWF enhances platelet spreading arterial subendothelium and consequently that the spreading is impaired in VWD. The enhancement may be caused directly by F VIII-VWF or indirectly as the result of a better attachment of contact platelets.
D001158:Arteries / Q000648:ultrastructure*; D001779:Blood Coagulation Factors / Q000378:metabolism*; D001792:Blood Platelets / Q000502:physiology*; D004727:Endothelium / Q000378:metabolism; D005169:Factor VIII / Q000378:metabolism*; D006801:Humans; D008854:Microscopy, Electron; D010973:Platelet Adhesiveness; D011485:Protein Binding; D013997:Time Factors; D014841:von Willebrand Factor / Q000378:metabolism*
D001779:Blood Coagulation Factors; D014841:von Willebrand Factor; D005169:Factor VIII